Effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on incidence and progress of posterior subcapsular opacities (PSO) associated with genetically influenced retinal degeneration are being studied in pink-eyed Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in retinal pigmented epithelium (RPE). Peroxidation in polyunsaturated fatty acids in debris lead to water-soluble toxic aldehydes detectable in the vitreous and toxic to lens cells and membranes. Dystrophic rats fed a natural ingredient diet (NIH-07) were highly sensitiv to retina light damage, beginning at an intensity of 10 to 40 lux, and 27 percent of the rats developed mature cataracts by 5 to 12 months. Rhodopsin bleaching is essential for retina light damage and PSO. In vitro free retinaldehyde has been shown to be a photosensitizer to generate singlet oxygen, an extremely damaging oxidant for both lipids and proteins, and this also may occur in vivo. In RCS rats reared at 10 to 40 lux, a purified diet (AIN-76A) fortified wit antioxidants (0.4 percent beta-carotene + 0.01 percent BHT) prevented PSO and mature cataracts. A diet containing additional antioxidants (1,000 mg/ diet of vitamin C and 150 mg/Kg vitamin E) retarded retinal degeneration during the time the cataracts would have had their onset (23 to 53 postnata days) if NIH-07 had been fed. Higher concentrations of vitamin E did not show additional retardation of retinal degeneration. Effects of increasing environmental lighting in incidence of bilateral matu cataracts were studied in pink-eyed RCS rats fed the NIH-07. Incidence of bilateral mature cataracts (BMC) was 5 percent in rats reared in 10 to 40 lux of cyclic light; but was 25 percent in rats reared in 110 lux of consta light; 70 percent in 270 lux of constant light; and 100 percent in 65-day-o rats given 48 hours of high intensity light (7500 lux). After lengthy or intense illumination, occurrence of disturbed meridional rows of lens epithelial cells and posterior nucleated (Wedl) cells pointed to proliferat n of germinative zone epithelial lens cells from deoxyribonucleic acid (DNA) damage. At low illumination, damage can be repaired (stationary cataracts and rare BMC). The results are consistent with the hypothesis of PSC causation by DNA damage to lens epithelial cells. Agents that can have thi effect include products of peroxidation of polyunsaturated fatty acids, sho wavelength radiation (UV, X-rays, beta and gamma rays) and numerous chemical mutagens such as N-nitroso-N-methylurea (NMU). Normal albino rats, injected with NMU at a concentration and dosage sufficient to cause breast cancer, developed BMC by 5 months of age. These cataracts were PSC of a more severe nature than ever seen in RCS rats (exposed to excessive light), with abnormally large cells (some binucleate) not only at the posterior pole but encircling the lens. The retinal showed advanced degeneration.